Disrupting Disease at the Cellular Source

Traditional brain cancer therapies often fail because they target the rapidly dividing cells of the tumor mass but leave behind a highly resilient subpopulation of cells known as Cancer Stem Cells (CSCs). These cells act as the fundamental source of the tumor, driving inevitable disease recurrence.

RR2 GBM cells treated with CT-179 in cell cycle arrest.
Image credit: Terrence Johns, PhD

GBM cancer cells with OLIG2 (green) in the nucleus of the cells.
Image credit: Human Protein Atlas, www.proteinatlas.org. Image available from v25.proteinatlas.org/ENSG00000205927-OLIG2/subcellular

The Role of OLIG2

In many aggressive CNS malignancies, the survival of CSCs is driven by a master control switch: the OLIG2 transcription factor. OLIG2 not only fuels the unchecked growth of these CSCs but also manipulates the tumor micro-environment, actively suppressing the body's natural immune response and hiding the tumor from attack.

OLIG2 Drives Proliferation, Invasion, and Immune Evasion

Glioma Stem Cell

Illustration of a spherical virus particle with a visible DNA double helix inside and protein structures.OLIG2 Dimer

Proliferation

Blue 3D model of a spherical virus particle with surface spikes on its shell.

Unchecked cell proliferation

Resistance

Suppresses p53/p21 pathway

Concept artwork for biosecurity and cancer biology: a blue shield with molecular clusters, surrounded by a pill, a stop sign, a key with a radiation symbol, and p53/p21 icons.

Chemo and radiation resistance

Invasion

Promotes invasion via TGFß2 signaling

Illustration of a blue immune cell attaching to a pink epithelial cell layer and releasing particles from it.

Invasion into healthy brain tissue

Immune Evasion

OLIG2-HDAC7 represses CXCL10 creating a cold microenvironment

Small blue virus particle circled on the left enlarging into a larger virus on the right, labeled OLIG2-HDAC7.

Cold Tumor Microenvironment

CT-179: A Dual-Action Breakthrough

Glioma Stem Cell

Cell interior showing a DNA double helix, a CT-179 drug molecule, and arrows indicating interaction with genetic sites.
Disrupts OLIG2 dimerization & Prevents DNA binding

Action 1: Direct Tumor Cell Effect

Disruption of OLIG2 dimerization

Diagram showing abnormal mitosis causing mitotic arrest on the left and apoptotic/mitotic catastrophe on the right, connected by an arrow.

Eradicating Cancer Stem Cells

CT-179 directly kills the OLIG2-expressing CSCs, destroying the primary source responsible for tumor recurrence.

Action 2: Immune Effect

Restoration of CXCL10 expression

Schematic of viral replication: blue particle cluster enters, several green viruses reproduce, resulting in blue and orange viral particles on the right.

Reversing Immune Suppression

By silencing OLIG2's influence on the microenvironment,

CT-179 reverses tumor-driven immune suppression, turning a "cold" tumor environment "hot" and equipping the body’s innate immune system to fight back.